Keratitis (corneal infection and inflammation) caused by herpes simplex virus (HSV) is a major cause of blindness from corneal scarring and opacity worldwide [1].

HSV keratitis typically presents as an infection of the superficial layer of the cornea, with punctate or diffuse branching (dendritic) lesions of the epithelium that do not usually involve the stroma. Applying topical glucocorticoid drops to the infected eye (without use of concomitant antiviral medication) can exacerbate the infection and potentially lead to involvement of deeper stromal structures with threat to vision [2].

Herpes simplex virology — Two clinically important herpes simplex virus (HSV) types exist in the subfamily alpha herpesviridae, HSV-1 and HSV-2. Humans are the only natural host for both types. HSV-1 accounts for most oral, labial, and ocular infections and HSV-2 for most genital infections, although there is considerable and increasing overlap in these distributions.

Primary infection with HSV-1 occurs following inoculation of mucosal or skin surfaces by direct contact. Most ocular disease is thought to represent recurrent HSV disease following the establishment of viral latency in the host, rather than a primary ocular infection. Latency develops after the virus enters sensory neurons and travels to sensory ganglia (usually the trigeminal ganglion for ocular disease) by retrograde axoplasmic flow [3]. The virus remains in ganglia for the lifetime of the host. It has been proposed that HSV-1 latency may also be established in the cornea, although this is controversial [4-6]. (See "Pathogenesis of herpes simplex virus type 1 infection".)

To continue reading this article, you must log in with your personal, hospital,
or group practice subscription. For more information or to purchase a personal subscription, click below on
the option that best describes you: